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1
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Interleukin 1beta induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells

100%
Uracz W., Uracz D., Olszanecki R., Gryglewski R. J.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 4,1
Prostaglandin endoperoxide H2 (PGH2) is generated from arachidonic acid by either constitutive (COX-1) or inducible (COX-2) cyclooxygenases. In arterial wall PGH2 is converted by PGI2 synthase (PGI-S) to prostacyclin (PGI2), and in platelets by thromboxane synthase (TX-S) to thromboxane (TXA2). Other prostanoids as PGD2, PGF2alpha or PGE2 were believed to arise non-enzymatically from PGH2. Only recently, human prostaglandin E synthase (PGE-S) has been identified and cloned as a membrane bound, microsomal, glutathione-dependent inducible enzyme. Here we demonstrated that interleukin 1ß (IL-1ß) is an inducer of COX-2 and PGE-S in human umbilical vein endothelial cells (HUVEC). Functional expression of PGE-S was measured at the level of specific mRNA by semi-quantitative RT-PCR, PGE-S protein was detected by Western blot in HUVEC, while PGE2 was measured by immunoassay in the supernatant. Actinomycin D, a classical transcription inhibitor, was used to prove that indeed IL-1ß induced the functional PGE-S enzyme. PGE2 generation in HUVEC was inhibited by indomethacin, acetamoniphen and dexamethasone. In conclusion, we found that in cultured endothelial cells IL-1ß induced as evidenced by the appearance of its transcript and its functional enzyme. The induction of endothelial PGE-S and COX-2 appeared to be and their transcripts were induced as fast as one might expect from immediate early genes. It means that IL-1ß-triggered-PGE2 biosynthesis in endothelial cells is probably regulated by induction of both COX-2 and PGE-S. This is way we hypothesise the existence of at least two distinct pools of COX-2: the first selectively coupled to PGE-S and the second one that is coupled to PGI-S yielding the main endothelial product - PGI2.
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Prostaglandin E receptor subtypes involved in stimulation of gastroduodenal bicarbonate secretion in rats and mice

84%
Takeuchi K., Ukawa H., Furukawa O., Kawauchi S., Araki H., Sugimoto Y., Ishikawa A., Ushikubi F., Narumiya S.
Journal of Physiology and Pharmacology
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1999
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tom 50
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nr 2
3
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Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update

67%
Dajani E. Z., Agrawal N. M.
Journal of Physiology and Pharmacology
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1995
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tom 46
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nr 1
4
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Involvement of prostaglandin E receptor EP3 subtype and prostacyclin IP receptor in decreased acid response in damaged stomach

67%
Nishio H., Terashima S., Nakashima M., Aihara E., Takeuchi K.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 3
We investigated the roles of cyclooxygenase (COX) isozymes and prostaglandin E (PGE) receptor EP1 and EP3 subtypes or prostacyclin IP receptors in the decrease in acid secretion in the damaged mouse stomach. Male C57/BL6 mice, both wild type and animals lacking EP1, EP3, or IP receptors, were used after 18 h of fasting. Under urethane anesthesia, the stomach was mounted on an ex-vivo chamber and perfused with saline, and acid secretion as well as transmucosal potential difference (PD) was measured before and after exposure to 20 mM taurocholate Na (TC) for 20 min. Indomethacin, SC-560 or rofecoxib was given i.d. 30 min before TC. Mucosal exposure to TC in wild-type mice caused a reduction in PD, followed by decrease in acid secretion. Indomethacin attenuated the decrease in acid secretion after exposure to TC in wild-type mice, an effect mimicked by SC-560 but not rofecoxib, yet none of these drugs affected the decrease in PD. An altered acid response after exposure to TC was similarly observed in EP1 (-/-) mice but mitigated in mice lacking either EP3 or IP receptors, although a decrease in PD was observed in all groups. Furthermore, the decreased acid response was also attenuated by prior administration of the EP3- but not EP1- antagonist. Mucosal levels of PGE2 and 6-keto PGF1alpha increased after exposure to TC in all groups of mice. In conclusion, the decrease in acid secretion in the damaged stomach is mediated by endogenous PGs derived from COX-1, through PGE2/EP3 receptors and prostacyclin/IP receptors.
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Prostaglandin E [dmPGE2] action in vitro on the activity of rat liver Golgi apparatus galactosyltransferase

67%
Kordowiak A. M., Tomecki J., Procyk K., Kapusta P.
Acta Biochimica Polonica
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1993
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tom 40
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nr 4
In vitro addition of 16,16'-dimethyl prostaglandin E2 to Golgi-rich membrane fraction in final concentration of 0.1 ng/1 mg of protein increased generally the activity of galactosyltransferase in comparison with control. The percentage of phospholipids in the whole fraction was similar in both investigated groups, only the sum of phosphatidylethanolamine + phosphatide acid was significantly lower after addition of dmPGE2 than in the control (0.001
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